KU-0063794

製品コードS1226

KU-0063794化学構造

分子量(MW):465.54

KU-0063794 is a potent and highly specific dual-mTOR inhibitor of mTORC1 and mTORC2 with IC50 of ~10 nM in cell-free assays; no effect on PI3Ks.

サイズ 価格(税別)  
JPY 29880.00
JPY 14940.00
JPY 28220.00
JPY 78020.00
JPY 111220.00
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バルク問合せ

カスタマーフィードバック(4)

  • Effects of PI3K and mTOR inhibitors on IGF1R and AKT signaling in RMS cells. Rh41 cells were treated with 0.3 uM PI3K inhibitor BKM120, 0.3 uM mTOR inhibitor KU0063794 for the indicated time. Lysates were made and analyzed for p-AKT, S6RP and IGF1R.

    Oncogene 2013 10.1038/onc.2013.509. KU-0063794 purchased from Selleck.

  •  

    mTORC2 is required for mechanical activation of Akt. A, immunoblots of mdMSC subjected to strain for 45 min following treatment with the mTOR inhibitor KU0063794 (2uM). B, densitometric analysis of phosphorylated GSK3 (Ser-9) normalized to total GSK3. D, immunoblots of mdMSC treated with KU0063794 and then stimulated with insulin (50 nM) for 60 min.

    J Biol Chem 2011 286, 39450-6. KU-0063794 purchased from Selleck.

  • mTORC2-mediated stretch-induced SGK-1 phosphorylation. SMCs infected with Ad-SGK-1 were pretreated with PPP (10 μmol/L), rapamycin (100 nmol/L),or Ku-0063794 (10 μmol/L) for 30 minutes and then were subjected to stretch or IGF-1 (10 ng/mL) for 30 minutes.

     

     

    Circ Res 2010 107, 1265-1274. KU-0063794 purchased from Selleck.

  • For MTT assays, cells (2,000 ~ 5,000 cells/well) were subcultured into 96-well plates according to their growth properties. Cell proliferation was assayed at 72 hr after treatment of KU-0063794 by adding 20 μl of 5 mg/ml 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) solution per 100 μl of growth medium. After incubating for 3-4 h at 37°C, the media were removed and 150 µl/well of MTT solvent (either absolute DMSO or isopropanol containing 4 μM HCl and 0.1% Nonidet-40) was added to dissolve the formazan. The absorbance of each well was measured by ELx808 (BioTek, Winooski, VT) or Wallac Victor2 (Perkin-Elmer Life Sciences, Boston, MA) Microplate Reader. Viable cells are presented as percent of control, vehicle-treated cells.

     

     

    Dr. Yong-Weon Yi from Georgetown University Medical Center. KU-0063794 purchased from Selleck.

製品安全説明書

mTOR阻害剤の選択性比較

生物活性

製品説明 KU-0063794 is a potent and highly specific dual-mTOR inhibitor of mTORC1 and mTORC2 with IC50 of ~10 nM in cell-free assays; no effect on PI3Ks.
ターゲット
mTORC1 [1]
(Cell-free assay)
mTORC2 [1]
(Cell-free assay)
~10 nM ~10 nM
体外試験

Compared with the mTOR inhibitor PP242, KU-0063794 exhibits higher specificity for mTOR, as being inactive against PI3Ks or 76 other kinases. In HEK-293 cells, KU-0063794 at 30 nM is sufficient to rapidly ablate S6K1 activity by blocking the phosphorylation of the hydrophobic motif (Thr389) and subsequently the phosphorylation of the T-loop residue (Thr229). In case of IGF1 stimulation of serum-starved HEK-293 cells, 300 nM of KU-0063794 is needed to inhibit the S6K1 activity by ~90%. KU-0063794 at 100-300 nM also completely inhibits the amino-acid-induced phosphorylation of S6K1 and S6 protein. Similar to S6K1, KU-0063794 inhibits the phosphorylation of mTORC1 at Ser2448 and mTORC2 at Ser2481 in a dose-dependent and time-dependent manner. In the presence of serum or following IGF1 stimulation, KU-0063794 induces a dose-dependent inhibition of the activity and phosphorylation of Akt at Ser473 and unexpected Thr308 as well as the phosphorylation of the Akt substrates PRAS40 at Thr246, GSK3α/GSK3β at Ser21/Ser9 and Foxo-1/3a at Thr24/Thr32. KU-0063794 but not rapamycin inhibits SGK1 activity and Ser422 phosphorylation as well as its physiological substrate NDGR1 in a dose-dependent manner, to the same extent as S6K1 and Akt phosphorylation, whereas KU-0063794 dose not inhibit phorbol ester induced ERK or RSK phosphorylation and RSK activation. Compared with rapamycin, KU-0063794 exhibits more significant potency to induce the complete dephosphorylation of 4E-BP1 at Thr37, Thr46 and Ser65. KU-0063794 inhibits cell growth of both wild-type and mLST8-deficient MEFs and induces a G1 cell cycle arrest, more significantly than rapamycin. [1]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HepG2  MUjD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MWWwMlHjiJN3MNMg{txO MWq3NkBp M{jQeYRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MmfCNlYzPzh6MUm=
HepG2  Mor0R49td267IF\vdo1ifGmxbjDBd5NigQ>? MV2x5qCUPTEEoN88US=> NGS3NY8yOCCm Mmja[IVkemWjc3XzJJRp\SCwdX3i[ZIhd2ZidnnhZoxmKEincFeyJINwdG:waXXzxsB{cWewaX\pZ4FvfGy7 MnPvNlYzPzh6MUm=
HepG2  NXyzb5RGSXCxcITvd4l{KEG|c3H5 MmG3NE4y6oDVNUFCpO69VQ>? M33Me|Q5KGh? M1THeYlv\HWlZYOgZZBweHSxc3nzJIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NYPNS4s5OjZ{N{i4NVk>
HepG2  NYS3b2x5TnWwY4Tpc44hSXO|YYm= M2DQdVUwOTBizszN MYeyOEBp MkOz[JJidWG2aXPhcIx6KGmwaHnibZR{KHCqb4PwbI9zgWyjdHnvckBw\iCDS2SgZZQhW2W{LUS3Ny=> NEKwcJozPjJ5OEixPS=>
HepG2  MXrGeY5kfGmxbjDBd5NigQ>? MnvzOU8yOCEQvF2= NHjpdmszPCCq MnHW[I94dnKnZ4XsZZRmeyC2aHWgcIV3\Wy|IFjJSlHPuSCjbnSgZ5lkdGmwIFSxxsA> M2TVb|I3Ojd6OEG5
HepG2  MWnGeY5kfGmxbjDBd5NigQ>? NH\3N28xNjIkgKO1NOKh|ryP NVXMR2pHOjRiaB?= NHL3ZYlqdmS3Y3XzJJA3OiCmb4fudoVofWyjdHnvckwhSmWlbHnuMVEh\XiycnXzd4lwdiCjbnSgUGM{Si2LIITvJGxEO0JvSVmgZ49vfmW{c3nvckBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MkSwNlYzPzh6MUm=
HepG3  NI\jTmpHfW6ldHnvckBCe3OjeR?= M3HWRVAvOeLCk{WwxsDPxE1? MlHMOFghcA>? NYDHUnFRcW6mdXPld{Bk\WyuIHH1eI9xcGGpeTDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= M3vKNlI3Ojd6OEG5
AGS M3W1PWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWLJR|UxRTF3LkCgxtEhOi57MTFOwG0> M3nuc|I1PTl5NEe4
HGC27 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUX4W2Q4UUN3ME2xOU4xKMLzIESuPFIh|ryP MXuyOFU6PzR5OB?=
MKN45 NYr1eGZuT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF;5eY5KSzVyPUCuPFIhyrFiMD6wNUDPxE1? MVuyOFU6PzR5OB?=
NUGC4 NXOxWINvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1XlcWlEPTB;Mj65N{DDuSByLkOxJO69VQ>? NHTENJMzPDV7N{S3PC=>
PC9 NUm2Z|dWT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mn;wO|IhcA>? NVjVWIhEUUN3ME2xNE4yPcLzMD62NkBvVQ>? NGnreJAzOzh5NEi4NC=>
PC9GR NIO3OXlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYf2VZNKPzJiaB?= MVfJR|UxRTZwMkJCtVEvOzBibl2= MV2yN|g4PDh6MB?=
H1650 NIfSdm5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWC3NkBp MV7JR|UxRTdwNkJCtVAvPjJibl2= MlS5NlM5PzR6OEC=
H1975 NH;nVXlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkjoO|IhcA>? NHKyfIVKSzVyPUGxMlE2yrFyLkmzJI5O M{fqdFI{QDd2OEiw
PC9 MkfPSpVv[3Srb36gRZN{[Xl? MV:xNE4yPSCwTR?= NWLRbGlrPzJiaB?= MVvpcohq[mm2czDtWG9TKHCqb4PwbI9zgWyjdHnvckB{fGG2dYRCpC=> M{TPXlI{QDd2OEiw
PC9GR NVX1XlAzTnWwY4Tpc44hSXO|YYm= NHTiWYg3NjJzIH7N Mne0O|IhcA>? NGjmWW5qdmirYnn0d{BuXE:UIIDoc5NxcG:{eXzheIlwdiC|dHH0eZPDqA>? MWeyN|g4PDh6MB?=
H1650 NWjVRXFKTnWwY4Tpc44hSXO|YYm= M1HFc|cvPjFibl2= MWS3NkBp NVHEeGRKcW6qaXLpeJMhdVSRUjDwbI9{eGixconsZZRqd25ic4TheJV{yqB? NXjnb5pkOjN6N{S4PFA>
H1975 NYPtNmdHTnWwY4Tpc44hSXO|YYm= M4O0RlEyNjF3IH7N MWS3NkBp NHrBTmVqdmirYnn0d{BuXE:UIIDoc5NxcG:{eXzheIlwdiC|dHH0eZPDqA>? MlvlNlM5PzR6OEC=
PC9 MXTGeY5kfGmxbjDBd5NigQ>? NITJfmEyOC5zNTDuUS=> M33G[|czKGh? MV\pcohq[mm2czDwbI9{eGixconsZZRqd25ib3[gdFcxWz[N M3rETFI{QDd2OEiw
PC9GR MWrGeY5kfGmxbjDBd5NigQ>? MnPzOk4zOSCwTR?= MV63NkBp NVn2[pozcW6qaXLpeJMheGixc4Doc5J6dGG2aX;uJI9nKHB5MGO2Ty=> M{f5b|I{QDd2OEiw
H1650 M1G1RmZ2dmO2aX;uJGF{e2G7 M4\YSVcvPjFibl2= NWXXUFBUPzJiaB?= NYDZU5cxcW6qaXLpeJMheGixc4Doc5J6dGG2aX;uJI9nKHB5MGO2Ty=> NY\LfIpSOjN6N{S4PFA>
H1975 NFLuUZdHfW6ldHnvckBCe3OjeR?= NX:0eoRsOTFwMUWgcm0> MUm3NkBp M1XMb4lvcGmkaYTzJJBpd3OyaH;yfYxifGmxbjDv[kBxPzCVNlu= MX2yN|g4PDh6MB?=
LNCaP MoKxR4VtdCCYaXHibYxqfHliQYPzZZk> M{PWcFAuOTBizszN NULzeZRzOjRiaNMg NYS3dGFt\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NX;CUFRYOjN6NEC2NFU>
PC-3 MmDyR4VtdCCYaXHibYxqfHliQYPzZZk> M4no[FAuOTBizszN NUS4XnNTOjRiaNMg NGDmN25l\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= NV\4NYtXOjN6NEC2NFU>
MDA-MB-468  M3fQ[WNmdGxiVnnhZoltcXS7IFHzd4F6 NYjISnJjOC1zMDFOwG0> M4Pp[VI1KGkEoB?= NV7scllk\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy MXmyN|g1ODZyNR?=
LNCaP M1\ndGZ2dmO2aX;uJGF{e2G7 MYmyNFDjiJN6MECgcm0> NHm1OmEzPCCqwrC= MXvk[YNz\WG|ZYOgeIhmKHCqb4PwbI9zgWyjdHnvckBt\X[nbDDv[kBxPzCVNlugbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= MnzSNlM5PDB4MEW=
PC-3 NIjDSJJHfW6ldHnvckBCe3OjeR?= MX[yNFDjiJN6MECgcm0> MUWyOEBpyqB? MlWw[IVkemWjc3XzJJRp\SCyaH;zdIhwenmuYYTpc44hdGW4ZXygc4YheDdyU{\LJIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NHTjWmgzOzh2ME[wOS=>
MDA-MB-468  NXzRO25xTnWwY4Tpc44hSXO|YYm= NEf6T2wzODEkgKO4NFAhdk1? M3iyfFI1KGkEoB?= M4PI[4Rm[3KnYYPld{B1cGVicHjvd5Bpd3K7bHH0bY9vKGyndnXsJI9nKHB5MGO2T{BqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> NX7ieYdvOjN6NEC2NFU>
Caki-1  M13wU2Z2dmO2aX;uJGF{e2G7 NX;4U5lXOTByLUKwNFAhdk1? MXSxNE0yQDBibXnu MV7EUXNQ NEfyc4lqdmirYnn0d{Bjd3SqIH3UU3JEOSCjbnSgcXRQWkN{IHHzJIlv\GmlYYTl[EBjgSC2aHWg[IVkemWjc3WgbY4heGixc4Doc5J6dGG2aX;uJI9nKGSxd37zeJJm[W1iZX\m[YN1d3K| M33kNVI{OzR7OUi5
786-O MYfGeY5kfGmxbjDBd5NigQ>? M1LkU|ExOC1{MECwJI5O M4\ve|ExNTF6MDDtbY4> NGDyWWNFVVOR MlXubY5pcWKrdIOgZo91cCCvVF;SR|Eh[W6mIH3UU3JEOiCjczDpcoRq[2G2ZXSgZpkhfGinIHTlZ5Jm[XOnIHnuJJBpd3OyaH;yfYxifGmxbjDv[kBld3ewc4Ty[YFuKGWoZnXjeI9zew>? NXz4dVIyOjN|NEm5PFk>
Caki-1  NYDkWJNYS2WubDDWbYFjcWyrdImgRZN{[Xl? NHnUTIQ{ODBvNECwNEBvVQ>? MV:yOE06PiCq NVKySppZTE2VTx?= M1LyWJN2eHC{ZYPz[ZMhfGinIHPlcIwhfmmjYnnsbZR6KGmwIHLveIghfGmvZTDhcoQh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ NYH4Zll1OjN|NEm5PFk>
786-O M1rwd2NmdGxiVnnhZoltcXS7IFHzd4F6 NHv3TWY{ODBvNECwNEBvVQ>? MWGyOE06PiCq NXTac2Y4TE2VTx?= MYjzeZBxemW|c3XzJJRp\SClZXzsJJZq[WKrbHn0fUBqdiCkb4ToJJRqdWViYX7kJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? MWCyN|M1QTl6OR?=
Caki-1  Mn;GSpVv[3Srb36gRZN{[Xl? NHviTnYzKML3TR?= NFPxVmE4OiCq MYHEUXNQ MWrpcoR2[2W|IFexJINmdGxiY4njcIUh[XK{ZYP0JIFv\CCjdYTvdIhi\3l? NYXEN2FPOjN|NEm5PFk>
786-O NHftXJdHfW6ldHnvckBCe3OjeR?= NEHkWVAzKML3TR?= MoDsO|IhcA>? NFjzdFRFVVOR Mk[1bY5lfWOnczDHNUBk\WyuIHP5Z4xmKGG{cnXzeEBidmRiYYX0c5Bp[We7 MlfwNlM{PDl7OEm=

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体内試験 Ku0063794 inhibits tumor growth and mTOR signaling in a preclinical renal cell carcinoma model. However, Ku0063794 was not more effective than temsirolimus in the animal study. A possible explanation for lack of greater activity in vivo for Ku0063794 is that temsirolimus has important effects on the tumor microenvironment. Temsirolimus decreased angiogenesis in the xenograft tumors while Ku0063794 did not. Temsirolimus treated tumors expressed less VEGF and PDGF than Ku0063794 treated tumors, thus stimulating less angiogenesis[2].

お薦めの試験操作(参考用のみ)

キナーゼ試験:

[1]

+ 展開

mTOR complexes kinase assays:

HEK-293 cells are freshly lysed in Hepes lysis buffer. Lysate (1-4 mg) is pre-cleared by incubating with 5-20 μL of Protein G-Sepharose conjugated to pre-immune IgG. The lysate extracts are then incubated with 5-20 μL of Protein G-Sepharose conjugated to 5-20 μg of either anti-Rictor or anti-Raptor antibody, or pre-immune IgG. All antibodies are covalently conjugated to Protein G-Sepharose. Immunoprecipitations are carried out for 1 hour at 4 °C on a vibrating platform. The immunoprecipitates are washed four times with Hepes lysis buffer, followed by two washes with Hepes kinase buffer. For Raptor immunoprecipitates used for phosphorylating S6K1, for the initial two wash steps the buffer includes 0.5 M NaCl to ensure optimal kinase activity. GST-Akt1 is isolated from serum-deprived HEK-293 cells incubated with PI-103 (1 μM for 1 hour). GST-S6K1 is purified from serum-deprived HEK-293 cells incubated with rapamycin (0.1 μM for 1 hour). mTOR reactions are initiated by adding 0.1 mM ATP and 10 mM MgCl2 in the presence of various concentrations of KU-0063794 and GST-Akt1 (0.5 μg) or GST-S6K1 (0.5 μg). Reaction are carried out for 30 minutes at 30 °C on a vibrating platform and stopped by addition of SDS sample buffer. Reaction mixtures are then filtered through a 0.22-μm-poresize Spin-X filter and samples are subjected to electrophoresis and immunoblot analysis with the indicated antibodies.
細胞試験:

[1]

+ 展開
  • 細胞株: Wild-type and mLST8 deficient MEFs
  • 濃度: Dissolved in DMSO, final concentration ~3 μM
  • 反応時間: 24, 48, and 72 hours
  • 実験の流れ:

    Cells are treated with KU-0063794 for 24, 48, and 72 hours, and the medium is changed every 24 hours with freshly dissolved KU-0063794. For the measurement of cell growth, cells are washed once with PBS, and fixed in 4% (v/v) paraformaldehyde in PBS for 15 minutes. After washing once with water, the cells are stained with 0.1% Crystal Violet in 10% ethanol for 20 minutes and washed three times with water. Crystal Violet is extracted from cells with 0.5 mL of 10% (v/v) ethanoic (acetic) acid for 20 minutes. The eluate is then diluted 1:10 in water and absorbance at 590 nm is quantified. For the assessment of cell cycle distribution, cells are harvested by trypsinization, washed once in PBS, and re-suspended in ice-cold aq. 70% (v/v) ethanol. Cells are washed twice in PBS plus 1% (w/v) BSA and stained for 20 minutes in PBS plus 0.1% (v/v) Triton X-100 containing 50 g/mL propidium iodide and 50 g/mL RNase A. The DNA content of cells is determined using a FACSCalibur flow cytometer and CellQuest software. Red fluorescence (585 nm) is acquired on a linear scale, and pulse width analysis is used to exclude doublets. Cell-cycle distribution is determined using FlowJo software.


    (参考用のみ)
動物試験:

[2]

+ 展開
  • 動物モデル: Nu/Nu nude mice
  • 製剤: one part DMSO and then diluted (200 µg/100 µl) with 4 parts PEG1500 (50% (w/v) in 75 mM Hepes, pH 8.0
  • 投薬量: 8 mg/kg
  • 投与方法: i.p.
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 16 mg/mL (34.36 mM)
Water Insoluble
Ethanol Insoluble
体内 左から(NMPから)右の順に溶剤を製品に加えます(文献ではなく、Selleckの実験によるデータ):
30% PEG400+0.5% Tween80+5% propylene glycol
混合させたのち直ちに使用することを推奨します。
30 mg/mL

* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程で起きる正常な現象ですからご安心ください。

化学情報

分子量 465.54
化学式

C25H31N5O4

CAS No. 938440-64-3
保管
in solvent
別名 N/A

便利ツール

モル濃度計算器

モル濃度計算器

求めたい質量、体積または濃度を計算してください。

質量 (g) = 濃度 (mol/L) x 体積 (L) x 分子量 (g/mol)

モル濃度計算器方程式

  • 質量
    濃度
    体積
    分子量

*貯蔵液を準備するとき、常に、オンであるとわかる製品のバッチに特有の分子量を使って、を通してラベルとMSDS/COA(製品ページで利用可能な)。

希釈計算器

希釈計算器

貯蔵液を準備するために必要な希釈率を計算してください。Selleck希釈計算器は、以下の方程式に基づきます:

開始濃度 x 開始体積 = 最終濃度 x 最終体積

希釈の計算式

この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 入力 出力 )

  • C1
    V1
    C2
    V2

常に貯蔵液を準備するとき、小びんラベルとMSDS/COA(オンラインで利用できる)で見つかる製品のバッチに特有の分子量を使ってください。

連続希釈計算器方程式

  • 連続希釈剤

  • 計算結果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
分子量計算器

分子量计算器

そのモル質量と元素組成を計算するために、合成物の化学式を入力してください:

総分子量:g/mol

チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2

モル濃度計算器

質量 濃度 体積 分子量

技術サポート

ストックの作り方、阻害剤の保管方法、細胞実験や動物実験の際に注意すべき点など、製品を取扱う時に問い合わせが多かった質問に対しては取扱説明書でお答えしています。

Handling Instructions

他に質問がある場合は、お気軽にお問い合わせください。

  • * 必須

mTORシグナル伝達経路

mTOR Inhibitors with Unique Features

相関mTOR製品

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細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID